Intracellular signaling pathways involved in the relaxin-induced proliferation of rat Sertoli cells.

@article{Nascimento2012IntracellularSP,
  title={Intracellular signaling pathways involved in the relaxin-induced proliferation of rat Sertoli cells.},
  author={Aline Rosa Nascimento and Maristela Taliari Pimenta and Tha{\'i}s F G Lucas and Carine Royer and Catarina Segreti Porto and Maria Fatima Magalh{\~a}es Lazari},
  journal={European journal of pharmacology},
  year={2012},
  volume={691 1-3},
  pages={283-91}
}
Regulation of Sertoli cell number is a key event to determine normal spermatogenesis. We have previously shown that relaxin and its G-protein coupled receptor RXFP1 are expressed in rat Sertoli cells, and that relaxin stimulates Sertoli cell proliferation. This study examined the mechanisms underlying the mitogenic effect of relaxin in a primary culture of Sertoli cells removed from testes of immature rats. Stimulation with exogenous relaxin increased Sertoli cell number and the expression of… CONTINUE READING

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Stimulation with exogenous relaxin increased Sertoli cell number and the expression of the proliferating cell nuclear antigen ( PCNA ) , but did not affect the mRNA level of the differentiation markers cadherins 1 and 2 .
Stimulation with exogenous relaxin increased Sertoli cell number and the expression of the proliferating cell nuclear antigen ( PCNA ) , but did not affect the mRNA level of the differentiation markers cadherins 1 and 2 .
Stimulation with exogenous relaxin increased Sertoli cell number and the expression of the proliferating cell nuclear antigen ( PCNA ) , but did not affect the mRNA level of the differentiation markers cadherins 1 and 2 .
In conclusion , the mitogenic effect of relaxin in Sertoli cell involves coupling to G(i ) and activation of both MEK / ERK1/2 and PI3K / AKT pathways .
Relaxin - induced Sertoli cell proliferation was blocked by inhibition of MEK / ERK1/2 or PI3K / AKT pathways , but not by inhibition of PKC or EGFR activity .
Relaxin - induced Sertoli cell proliferation was blocked by inhibition of MEK / ERK1/2 or PI3K / AKT pathways , but not by inhibition of PKC or EGFR activity .
In conclusion , the mitogenic effect of relaxin in Sertoli cell involves coupling to G(i ) and activation of both MEK / ERK1/2 and PI3K / AKT pathways .
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